Faculty Profile: Qing Lu, DVM, PhD

Qing Lu
Qing Lu, DVM, PhD
Assistant Professor of Medicine (Research)
Bio Med Medicine
Work: +1 401-273-7100
Vascular endothelial cells, a monolayer lining the inner wall of blood vessels, play a crucial role in human health and disease. Abnormal lung vascular endothelial cell apoptosis leads to severe lung diseases, such as emphysema and pulmonary artery hypertension (PAH). The focus of Dr. Lu's study is to understand the regulation of lung endothelial cell apoptosis, particularly by transforming growth factor-beta1 signaling, and its role in the pathogenesis of PAH and cigarette smoke-induced emphysema. The experimental approches include both cultured cells and animal models.


Qing Lu, PhD, is Assistant Professor of Medicine (Research) at Brown Medical School. Dr. Lu received PhD from Institute of Zoology at the Chinese Academy of Sciences in 1999. She completed 3 years of post-doctoral training in the area of Reproductive Biology and Molecular Biology at University of Michigan Medical School. Dr. Lu joined the Vascular Research Laboratory at Brown Medical School as a Research Associate in 2002 and was then appointed to the Brown faculty as Instructor of Medicine (Research) in 2003. She was subsequently appointed Assistant Professor of Medicine (Research) at Brown Medical School in 2004.



Research Description

Transforming growth factor (TGF)-beta1, a member of TGF-beta superfamily, is a multifunctional cytokine that regulates numerous cellular functions. Abnormality of TGF-beta1 signaling has been implicated in several lung diseases, such as lung edema, emphysema, and pulmonary artery hypertension (PAH). Using cultured lung macro- and micro-vascular endothelial cells, Dr. Lu will elucidate the molecular mechanism(s) by which TGF-beta1 regulates lung endothelial monolayer permeability, endothelial cell proliferation, and endothelial cell apoptosis. Using animal models of PAH induced by hypoxia and hypoxia plus SU5416, Dr. Lu will investigate the role of TGF-beta1 siganling in the development of PAH. Recently, Dr. Lu has started a new project investigating the role of TGF-beta1 signaling in the pathogenesis of cigarette smoke-induced emphysema, using cigarette smoked animal models. The overall objective of her research is to understand the role of TGF-beta1 in the pathogenesis of these severe lung diseases and hopefully to obtain novel approaches for treatment and prevention these lung diseases.

Grants and Awards

BEST POSTER SUBMITTED BY A NEW INVESTIGATOR by the RI Science and Technology Advisory Council (STAC) and the statewide network of EPSCoR, INBRE, CTSA and COBRE investigators at the STAC meeting on June 3, 2008.
Research Award, ATS/Pulmonary Hypertension Association, 2008-2009
Fellow, Francis Family Foundation, 2004-2007
Research Award, American Lung Association, 2004-2006
Medical Research Award, Rhode Island Foundation, 2004
Weihua Science and Technology Award, The Chinese Academy of Sciences, 1999
Distinguished Graduate Student Achievement Award,The Chinese Academy of Sciences, 1998
Distinguished Graduate Student Achievement Award, Nanjing Agricultural University, China, 1995
Science and Technology Progress Award, Anhui Province, China, 1992
Science and Technology Progress Award, Hefei City, Anhui Province, China, 1992


4/2007, member, American Heart Association Northeast Consortium 1B peer review committee
4/2008, Member, American Heart Association REGION I Molecular Signaling 2 Study Group, peer review committee
Alternate Member, Research and Development Committee, Providence Veterans Affairs (VA) Medical Center, 2004
Member, Research and Development Committee, Providence VA Medical Center, 2005-2007
Member, Institutional Animal Care and Use Committee (IACUC), Providence VA Medical Center, 2005-present
Member, Zhi-Zhan Gu's Ph.D. Thesis Committee, 2005-2007

Funded Research

PI: Qing Lu
Agency: American Thoracic Society/Pulmonary Hypertension Association
"TGF-beta1 and Pulmonary Artery Hypertension"
Type: Research grant
Period: 1/1/08-12/31/09
Total direct costs: $100,000

PI: Qing Lu
Agency: Francis Family Foundation
"TGF-beta1 and endothelial monolayer permeability"
Type: Parker B. Francis Fellowship
Period: 7/1/04-6/30/07
Total direct costs: $126,000

PI: Qing Lu
Agency: American Lung Association
"The mechanism of TGF-beta1 regulation of endothelial monolayer permeability"
Type: Research Grant
Period: 7/1/04-6/30/06
Total direct costs: $70,000

PI: Qing Lu
Agency: Rhode Island Foundation
"TGF-beta1 and endothelial monolayer permeability"
Type: Medical Research Grant
Period: 1/1/04-12/31/04
Total direct costs: $10,000

PI: Sharon Rounds
Agency: National Heart, Lung, and Blood Institute (NHLBI)
"Small GTPases and Lung Endothelial Apoptosis"
Type: RO-1 HL 64936
Period: 4/1/06-3/31/11
Annual Direct Costs: $200,000
Role: co-investigator

Selected Publications

  • Lu Q (corresponding author), Patel B, Harrington EO, and Rounds S. TGF-β1 causes pulmonary microvascular endothelial cells apoptosis via ALK5. American Journal of Physiology Lung Cellular and Molecular Physiology. 296: L825–L838, 2009. (2009)
  • Lu Q and Rounds S. Pulmonary endothelial cell death: implications for lung disease pathogenesis. In: The Pulmonary Endothelium: Function in health and disease. Edited by N. F. Voelkel and S. Rounds. John Wiley & Sons, Ltd. Chichester, UK, p.243-260, 2009. (2009)
  • Lu Q (corresponding author). Transforming growth factor-beta1 protects against pulmonary artery endothelial cell apoptosis via ALK5. American Journal of Physiology: Lung Cellular and Molecular Physiology. 295, L123-L133, 2008. (2008)
  • Rounds S, Lu Q, Harrington EO, Newton J, and Casserly B. Pulmonary endothelial cell signaling and function. Transactions of the American Clinical and Climatological Association. 119:155-67, 2008. (2008)
  • Harrington EO, Lu Q, and Rounds S. Endothelial Cell Apoptosis. In: Endothelial Biomedicine. Edited by W. C. Aird, Cambridge University Press, New York, NY, pp1081-1097, 2007. (2007)
  • Lu Q, Harrington EO, Newton J, Jankowich M, and Rounds S. Inhibition of ICMT induces endothelial cell apoptosis through GRP94. American Journal of Respiratory Cell and Molecular Biology, 37: 20-30, 2007. (2007)
  • Lu Q (corresponding author), Harrington EO, Jackson H, Shannon CJ, Morin N and Rounds S. Transforming growth factor-beta1-induced endothelial barrier dysfunction involves SMAD2-dependent p38 activation and subsequent RhoA activation. Journal of Applied Physiology, 101, 375-384, 2006. (2006)
  • Lu Q, Harrington EO and Rounds S. Apoptosis and lung injury. Keio Journal of Medicine. 54 (4): 184-189, 2005. (2005)
  • Harrington EO, Shannon CJ, Morin N, Rowlett H, Murphy C. and Lu Q. PKCdelta regulates endothelial basal barrier function through modulation of RhoA GTPase activity. Experimental Cell Research, 308: 407-421, 2005. (2005)
  • Rounds S, Harrington EO, and Lu Q. Carboxyl methylation of small GTPases and endothelial cell function. In: J. Bhattacharya (Ed.), Cell Signaling in Vascular Inflammation, Humana Press, Totowa, NJ, pp 52-60, 2005. (2005)
  • Lu Q, Harrington EO, Hai C-M, Newton J, Garber M, Hirase T and Rounds S. Isoprenylcysteine carboxyl methyltransferase modulates endothelial monolayer permeability: involvement of RhoA carboxyl methylation. Circulation Research, 94: 306-315, 2004 (2004)
  • Kramer K, Harrington EO, Lu Q, Bellas R, Newton J, Sheahan KL and Rounds S. Isoprenylcysteine carboxyl methytransferase activity modulates endothelial cell apoptosis. Molecular Biology of the Cell, 14: 848-857, 2003 (2003)
  • Lu Q, Hutchins AE, Doyle CM, Lundblad JR and Kwok RPS. Acetylation of CREB by CBP enhances CREB-dependent transcription. The Journal of Biological Chemistry, 278: 15727-15734, 2003 (2003)
  • Lu Q, Smith GD, Chen DY, Han ZM and Sun QY. Activation of protein kinase C induces mitogen-activated protein kinase dephosphorylation and pronucleus formation in rat oocytes. Biology of Reproduction, 67: 64-69, 2002 (2002)
  • Lu Q, Dunn RL, Angeles R and Smith GD. Regulation of spindle formation by active mitogen-activated protein kinase and protein phosphatase 2A during mouse oocyte meiosis. Biology of Reproduction, 66: 29-37, 2002 (2002)
  • Lu Q, Smith GD, Chen DY, Yang Z, Han ZM, Schatten H and Sun QY. Phosphorylation of mitogen-activated protein kinase is regulated by protein kinase C, cyclic 3, 5-adenosine monophosphate, and protein phosphatase modulators during meiosis resumption in rat oocytes. Biology of Reproduction, 64: 1444-1450, 2001 (2001)
  • Sun QY*, Lu Q*, Breitbart H and Chen DY. cAMP inhibits mitogen-activated protein (MAP) kinase activation and resumption of meiosis, but exerts no effects after spontaneous germinal vesicle breakdown (GVBD) in mouse oocytes. Reproduction, Fertility and Development, 11: 81-86, 1999. (1999)
  • Lu Q, Sun QY, Breitbart H and Chen DY. Expression and phosphorylation of mitogen-activated protein kinase during spermatogenesis and epididymal sperm maturation in mice. Archives of Andrology, 43: 55-66, 1999 (1999)
  • * indicates equal contribution. ()
  • Lu Q*, Jankowich M*, Newton J, Harrington EO, and Rounds S. Alterations in molecular chaperones and eIF2α during lung endothelial apoptosis, American Journal of Physiology Lung Cellular and Molecular Physiology, under review. ()
  • Lu Q *, Harrington EO*, Newton J, Casserly B, Radin G, Warburton R, Zhou Y, Blackburn MR, and Rounds S. Adenosine protected against pulmonary edema through transporter- and receptor 2-mediated endothelial barrier enhancement. American Journal of Physiology Lung Cellular and Molecular Physiology, under revision. ()